1. Field of the Invention
The present invention relates generally to cardiac pacemakers, and more particularly to an implantable cardiac pacemaker including means for verifying that the pacing pulses generated by the pacemaker are producing the desired stimulation of the patient's heart.
2. Relevant Background
In the normal human heart, the sinoatrial (S-A) node, generally located near the junction of the superior vena cava and the right atrium, constitutes the primary natural pacemaker by which rhythmic electrical excitation is developed. The cardiac impulse arising from the S-A node is transmitted to the two atrial chambers, or atria, at the right and left sides of the heart. In response to this excitation, the atria contract, pumping blood from those chambers into the respective ventricular chambers, or ventricles.
The impulse is transmitted to the ventricles through the atrioventricular (A-V) node, or junction, which imposes a delay, and via a conduction system comprising the bundle of His, or common bundle, the right and left bundle branches, and the Purkinje fibers. In response, the ventricles contract, the right ventricle pumping unoxygenated blood through the pulmonary artery to the lungs and the left ventricle pumping oxygenated (arterial) blood through the aorta and the lesser arteries to the body.
The right atrium receives the venous (unoxygenated) blood from the upper part of the body (head, neck and chest) via the superior vena cava, or upper great vein, and from the lower part of the body (abdomen and legs) via the inferior vena cava, or lower great vein. The blood oxygenated by the lungs is carried via the pulmonary veins to the left atrium.
This action is repeated in a rhythmic cardiac cycle in which the atrial and ventricular chambers alternately contract and pump, then relax and fill. One-way valves along the veins, between the atrial and ventricular chambers in the right and left sides of the heart (the tricuspid valve and the mitral valve, respectively), and at the exits of the right and left ventricles (the pulmonary and aortic valves, respectively) prevent backflow of the blood as it moves through the heart and the circulatory system.
The S-A node is spontaneously rhythmic, and the cardiac rhythm originating from that primary natural pacemaker is termed "sinus rhythm". This capacity to produce spontaneous cardiac impulses is called "rhythmicity", or "automaticity". Some other cardiac tissues possess this electro-physiologic property and hence constitute secondary natural pacemakers, but the S-A node is the primary pacemaker because it has the fastest spontaneous rate. The secondary pacemakers tend to be inhibited by the more rapid rate at which impulses are generated by the sinus node.
Disruption of the natural pacemaking and propagation system occurs as a result of aging or disease, and is commonly treated by artificial cardiac pacing. Rhythmic electrical discharges of an implanted pacemaker are set at a desired rate and are applied to the heart as necessary to effect stimulation. In its simplest form, the pacemaker consists of a pulse generator powered by a self-contained battery pack, and a lead including at least one stimulating electrode electrically connected to the pulse generator. The lead is typically of the catheter type for intravenous insertion to position the stimulating electrode(s) for delivery of electrical impulses to excitable myocardial tissue in the appropriate chamber(s) in the right side of the patient's heart. Usually, the pulse generator is surgically implanted in a subcutaneous pouch in the patient's chest. In operation, the electrical stimuli are delivered to the excitable cardiac tissue via an electrical circuit that includes the stimulating and reference (indifferent) electrodes, and the body tissue and fluids.
A pacemaker operates in one of three different response modes, namely, asynchronous (fixed rate), inhibited (stimulus generated in absence of specified cardiac activity), or triggered (stimulus delivered in response to specified cardiac activity). The demand ventricular pacemaker, so termed because it operates only on demand, has been the most widely used type. It senses the patient's natural heart rate and applies stimuli only during periods when that rate falls below the preset pacing rate.
Pacemakers range from the simple fixed rate device that provides pacing with no sensing function, to the highly complex model implemented to provide fully automatic dual chamber pacing and sensing functions. The latter type of pacemaker is the latest in a progression toward physiologic pacing, that is, the mode of pacing that restores cardiac function as much as possible toward natural pacing.
Regardless of the particular type of pacemaker that may be employed to pace the patient's heart, it is essential to ascertain that the pacing pulse applied via the implanted electrode assembly is indeed stimulating the heart. That is to say, the pulse in conjunction with the implanted cathodic electrode must impress an electric field of sufficient field strength and current density on the excitable myocardial tissue at the electrode site to initiate depolarization of the tissue and the spreading of a so-called action potential. When that happens, the chamber in which the cathodic electrode is implanted undergoes contraction in the same manner as would a healthy heart under the influence of the natural physiologic pacing system. This stimulation of the heart, in which a pulse generated by a cardiac pacemaker causes contraction of the selected chamber(s) is termed "capture." The means or method by which it is ascertained that the pacemaker stimuli are achieving capture of the heart is called "capture verification."
It is a principal object of the present invention to provide a pacemaker having an improved means and method for capture verification.
In general, capture verification techniques are based on detecting the potential evoked when the heart is captured. If capture has not occurred, there will be no evoked potential. It follows that each time the heart is paced, the cardiac signal may be monitored after a suitable delay to detect the presence of the evoked potential, and thereby to verify capture. In practice, however, reliable capture verification is not quite so simple, for many reasons, some of the more important being the small amplitude of the atrial signal, the signal masking attributable to electrode polarization (a signal-to-noise problem), and the relative difference between frequencies present in the atrial and ventricular signals.
Accordingly, it is another broad object of the present invention to provide a technique for capture verification which surmounts the usual impediments to sensing the potential evoked as a result of capture.